[Pulmonary anti-Aspergillus defences]

The lung, constantly exposed to inhaled infectious particles, uses a very efficient immune system to insure sterility of the airways. It has to be tightly regulated for the tissues to be kept from its potentially deleterious effects. Pulmonary anti-Aspergillus defences are based upon the concurrent action of innate immunity, non specific but rapidly mobilisable, and of adaptative immunity. The former first consists in natural barriers, namely the respiratory epithelium and its antimicrobial peptides (complement, defensins, collectins). Then come the phagocytic cells (macrophages and neutrophils), but also the dendritic cells, able to stimulate adaptative responses through the presentation of antigens they have phagocytised ans processed. The Toll-like receptors are among the key ones involved in the recognition of fungal components. Chemokines have a crucial role for the recruitment, maturation and activation of neutrophils, while anti-inflammatory cytokines tightly influence T lymphocytes functional differentiation. These latter, cornerstones of the adaptative immunity, differentiate into two mutually exclusive pathways according to the type of cytokines which they produce. The Th1 one is largely protective in the context of Aspergillus, while the Th2 one is deleterious. However, a good cooperation between these 2 pathways is required for an efficient protection. Pulmonary anti-Aspergillus defences are multifactorial. Innate immunity is crucial but a capacity of the host to generate specific responses is also warranted.